Posts Tagged methylphenidate

[ARTICLE] Follow-up after 5.5 years of treatment with methylphenidate for mental fatigue and cognitive function after a mild traumatic brain injury – Full Text

Objective: Prolonged mental fatigue and cognitive impairments are common after a mild traumatic brain injury (TBI). This sets limits for rehabilitation and for regaining the capacity for work and participation in social life.

Method: This follow-up study, over a period of approximately 5.5 years was designed to evaluate the effect and safety of methylphenidate treatment for mental fatigue after a mild TBI. A comparison was made between those who had continued, and those who had discontinued the treatment. The effect was also evaluated after a four-week treatment break.

Results: Significant improvement in mental fatigue, depression, and anxiety for the group treated with methylphenidate (p < .001) was found, while no significant change was found for the group without methylphenidate. The methylphenidate treatment group also improved their processing speed (p = .008). Withdrawal produced a pronounced and significant deterioration in mental fatigue, depression, and anxiety and a slower processing speed. This indicates that the methylphenidate effect is reversible if discontinued and that continued methylphenidate treatment can be a prerequisite for long-term improvement. The effect was found to be stable and safe over the years.

Conclusion: We suggest methylphenidate to be a possible treatment option for patients with post-TBI symptoms including mental fatigue and cognitive symptoms.

Introduction

Long-term mental fatigue and cognitive impairment are common after a mild, moderate or severe traumatic brain injury (TBI) and these can have a significant impact on work, well-being and quality of life (1). Fatigue and concentration deficits are acknowledged as being one of the most distressing and long-lasting symptoms following mild TBI (1). There is currently no approved treatment (2), although the most widely used research drug for cognitive impairments after TBI is methylphenidate (3). A few studies have used methylphenidate for mental fatigue after TBI with promising results including our own (4,5). Other clinical trials of drugs have reported improvements in mental fatigue ((−)-osu6162 (6)) or none ((−)-osu616, modafinil (79)).

In our feasibility study of methylphenidate (not placebo controlled) we reported decreased mental fatigue, improved processing speed and enhanced well-being with a “normal” dose of methylphenidate compared to no methylphenidate for people suffering from post-traumatic brain injury symptoms (4). We tested methylphenidate in two different dosages and found that the higher dose (20 mg three times/day) had the better effect compared to the lower dose. We also found methylphenidate to be well tolerated by 80% of the participants. Adverse events were reported as mild and the most commonly reported side-effects included restlessness, anxiety, headache, and increased heart rate; no dependence or misuse were detected (10). However, a careful monitoring for adverse effects is needed, as many patients with TBI are sensitive to psychotropic medications (11).

Participants who experienced a positive effect with methylphenidate were allowed to continue the treatment. We have reported the long-term positive effects on mental fatigue and processing speed after 6 months (12) and 2 years (13). No serious adverse events were reported (13)(Figure 1). In a 30-week double-blind-randomized placebo-controlled trial, Zhang et al. reported that methylphenidate decreased mental fatigue and improved cognitive function in the participants who had suffered a TBI. Moreover, social and rehabilitation capacity and well-being were improved (5). Other studies evaluating methylphenidate treatment after TBI have focused only on cognitive function reporting improved cognitive function with faster information processing speed and enhanced working memory and attention span (1421). A single dose of methylphenidate improved cognitive function and brain functionality compared to placebo in participants suffering from post-TBI symptoms (22,23). Most of these have been short-term studies covering a period between 1 day and 6 weeks and included participants suffering from mild or more severe brain injuries.

This clinical follow-up study was designed to evaluate the long-term effect and safety of methylphenidate treatment. We also evaluated the effect after a four-week treatment break and compared the subjective and objective effects with and without methylphenidate. Patients who had discontinued methylphenidate during this long-term study were also included in this follow-up, as it was our intention to compare the long-term effects on mental fatigue in patients with and without methylphenidate treatment.

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Continue —->  Follow-up after 5.5 years of treatment with methylphenidate for mental fatigue and cognitive function after a mild traumatic brain injury: Brain Injury: Vol 0, No 0

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[ARTICLE] Pharmacological management of long-term aggression secondary to traumatic brain injuries

Abstract
Aggression is common after traumatic brain injuries (TBI) in acute and chronic settings. However, there is limited guidance regarding its assessment and effective management. Whilst a number of pharmacological options are available for long term treatment, the evidence base is not of an adequate strength to support a unified practice. This article will explore the currently available guidelines and recommendations for treating chronic aggression after TBIs and evaluate the evidence for its pharmacological management.


Introduction

Aggression is a long term neurobehavioural sequelae of TBIs with incidences quoted from 11.5-33.7%.1 In TBI patients, aggressive behaviour tends to be impulsive rather than premeditated and can manifest as episodic dyscontrol syndrome, disinhibition or exacerbated premorbid antisocial traits.2 The underlying mechanisms of aggression are complex allowing numerous and diverse interventions targeting various pathways.

In acute settings, Lombard and Zafonte (2005) describe non-pharmacological measures to manage aggression including environmental alterations and ensuring minimal or non-contact restraints. Screening for systemic causes, optimising pain control and patients’ sleep-wake cycle are also advocated. In the event of failed non-pharmacological treatment, Lombard and Zafonte (2005) recommend that medication choice should be tailored to individuals; with side effect profiles taken into consideration.3

For chronic aggression, psychological therapies are used as a first line with pharmacological interventions trialled in later stages.4 Psychological therapy options include cognitive behavioural therapy (CBT), behavioural management utilising operant learning theory and contingency management. However, a review by Alderman (2013) concluded that further evidence using scientific methods is needed to analyse these approaches.5  Comparatively, there is a diverse body of literature addressing long term pharmacological treatment although quality among studies are varied. This article will focus on the aetiology for chronic post TBI aggression, current management guidelines and the evidence for long term pharmacological interventions.

Aetiology

Post TBI aggression has been associated with lesions affecting the prefrontal cortex – particularly the orbitofrontal and ventromedial areas – causing a loss of behavioural regulation. Disruption to inhibitory pathways between the prefrontal cortex and limbic system also results in limbic kindling and inappropriate emotional responses to negative stimuli thus facilitating aggressive behaviour.2 Associated neurotransmitter abnormalities include low cortical serotonin and impaired gamma amino-butyric acid (GABA)/ glutamate levels.6 Altered catecholamine and cholinergic levels are associated with cognitive impairment2 thus distorting information processing and predisposing patients to aggression.6 In TBI patients, underlying anxiety, affective disorders, seizures and frontal lobe dysfunction also increase susceptibility.10

Differentials for aggression

When identifying a cause for chronic aggressive behaviour, a patient’s previous experiences, comorbid psychiatric conditions and alcohol and/or substance abuse must be established with a collateral history.2,7  McAllister (2008) highlights the importance of determining pre-injury behaviour in order to exclude the possibility of symptoms being an exaggeration of pre-injury personality traits.8 Additionally, psychosocial factors must be deduced to identify possible triggers.2,7

Clinicians must be aware that aggression can be a presenting feature of other psychiatric disorders. Depression has a prevalence of 18.5% to 61% in post-TBI patients  and is linked with aggression due to their shared association with frontal lobe lesions and serotonin level imbalance.9 Other differentials include manic disorders (which can involve a more marked aggressive component if secondary to TBIs), anxiety disorders and alcohol and/or substance abuse. Personality and behavioural disorders such as affective lability, behavioural disinhibition and acquired antisocial behaviour should also be considered.8

Management guidelines

The National Institute for Health and Care Excellence (NICE) refers to the Scottish Intercollegiate Guidelines Network (SIGN) for rehabilitating patients with acquired brain injuries (ABIs). Psychological treatments advocated by SIGN include CBT, contingency management procedures, music therapy and comprehensive neurobehavioural rehabilitation (CNR).10 Family involvement appears to be associated with better outcomes2 and is also recommended.10

Of the studies quoted by SIGN, CNR was found to cause a positive effect in ABI patients in one systematic review although inconsistent results were obtained for the other three methods. Regarding pharmacological treatment, SIGN advises propranolol and pindolol as first line options.10

Pharmacological treatment

The aberrant neurotransmitter changes in the cortex and limbic areas as a result of TBIs2 provide targets for pharmacological therapy (as summarised in Table 1). Theoretically, cortical behavioural regulation can be enhanced by serotonergic agents and antagonists of dopaminergic and noradrenergic neurotransmission. Limbic hyperactivity can be dampened by the use of gamma aminobutyric acid (GABA) agonists, glutamatergic antagonists and anticholinergics.6

Impaired behavioural regulation

Antidepressants

Selective serotonin reuptake inhibitors (SSRIs) are indicated for their increase in dopamine and serotonin availability and the treatment of depression contributing to aggressive behaviour. In a trial conducted by Kant et al (1998), sertraline reduced aggression within one week of treatment although TBI severities were variable within the population.11 These results are mirrored in other trials presenting sertraline as a viable treatment option.12 Citalopram used in conjunction with carbamazepine successfully treated behavioural symptoms in a clinical trial of 22 patients conducted by Perino et al (2001)13 although the separate effects of both drugs are impossible to differentiate. A case study by Sloan et al (1992) found that fluoxetine improved emotional lability in one patient within a week.13

Tricyclic antidepressants have been shown to be useful for managing both post-traumatic and chronic aggression. Amitriptyline has reduced aggression with good tolerability despite its strong anticholinergic side effects in several studies and is suggested as the best option for treating behavioural disorders secondary to frontal lobe injuries without impairing cognition.13

Antipsychotics

There is a wide body of literature advocating antipsychotics for managing aggression due to their sedative effects.13 Nevertheless, the cognitive and extrapyramidal side effects of typical antipsychotics limit their value for chronic use. Comparatively, atypical antipsychotics have a milder side effect profile and are preferred although their cognitive impact in TBI patients is unclear.2 Furthermore, unlike older generations, atypical antipsychotics antagonise 5HT2 receptors and are therefore implicated in reduced aggression.9

Of the typical antipsychotics, chlorpromazine reduced explosiveness in one case study conducted by Sandel et al (1993). Various case studies also report haloperidol improving chronic agitation in TBI patients although significant side effects were encountered.13 Of the atypical antipsychotics the level of evidence is low. Quetiapine reduced aggression and irritability in seven patients in a trial conducted by Kim and Bijlani (2006).11 Olanzapine significantly reduced aggression within six months in a case study conducted by Umansky and Geller (2000). Clozapine was associated with varying levels of improvement in six case studies conducted by Michals et al (1993) however seizures were experienced in two patients.13

Overall, there is no reliable evidence advocating antipsychotic use for managing chronic post-TBI aggression. If antipsychotics are commenced for this purpose, it is suggested that their use is restricted to patients with psychosis.13

Beta blockers

Beta blockers are useful for cases where aggression is caused by underlying anxiety13 due to its inhibition of noradrenergic levels.9 A Cochrane review of four RCTs found that pindolol and propranolol reduced aggression within two to six weeks of starting treatment in ABI patients however no recommendations were made due to heterogeneity between samples, a small number of trials and small sample sizes.  The authors acknowledge that the trials involved high doses and so recommend caution when prescribing beta blockers for aggression.4

Methylphenidate

Methylphenidate is a psychostimulant indicated for its enhancement of dopamine and noradrenaline in the frontal lobe improving arousal and alertness.13 Mooney (1993) found in a single RCT that methylphenidate significantly improved anger scores in TBI patients.4 However other studies have yielded mixed results12,13 and no firm conclusion can be made.

Amantadine

Amantadine increases dopamine availability and acts on glutamatergic pathways. An advantage of its use is its non-sedating qualities however there is contradicting evidence for its efficacy.13 An RCT conducted by Schneider (1999) found no significant improvement4 however the trial was limited by a small sample size and large heterogeneity. Interestingly, studies of a lower level of evidence demonstrate favourable results.13 Due to this variability, its efficacy is still in question.

Buspirone

Buspirone – a serotonergic agonist licensed for treating anxiety13 – has also reduced aggression in several case studies2,12,14 warranting further research. Its side effects are amenable for use in TBIs although one disadvantage is its delayed onset.13

Hyperactive limbic drive

Anticonvulsants

The mood stabilising effects of anticonvulsants are mediated through their enhancement of GABA transmission.2 Carbamazepine has been demonstrated in studies to be effective for managing acute and chronic post- TBI aggression.12,13 Its side effects include impaired balance, sedation13 and cognitive impairment particularly in brain injured patients2 due to their heightened sensitivity. In a trial conducted by Mattes (2005), Oxcarbazepine reduced impulsive aggression however the number of TBI participants in the sample was unclear. Nine of the 48 participants also dropped out due to adverse effects11 suggesting more research is needed into its tolerability in TBI patients. Valproate has also been demonstrated to effectively manage behavioural and affective disorders13 with a milder cognitive impact compared to carbamazepine.2 Regarding other anticonvulsants, the evidence is of a lower standard. Pachet et al (2003) found that lamotrigine reduced aggression with good tolerability in one case study.11 Topiramate has been demonstrated to effectively treat manic symptoms but due to its side effects of psychosis and cognitive impairment,2 may be inappropriate for TBI patients. Case reports reference lithium to reduce post – TBI agitation however it may be unsuitable as a first line option due to its neurotoxicity.13

Benzodiazepines

Benzodiazepines are indicated for their anticonvulsive, anti-anxiety and sedative qualities facilitated by stimulation of the GABA receptor.13 There is limited literature on their chronic use in TBI patients due to their side effects of agitation, cognitive impairment and tolerance2 thus they are recommended to be more appropriate for cases of acute agitation or anxiety.11

Conclusion

There are many challenges in assessing and managing chronic aggression due to its complex aetiology. Previous literature presents a selection of pharmacological options however, their effect on TBI patients has not been confirmed resulting in limited guidance. The heterogeneity between samples also renders it impossible to predict treatment outcomes in the TBI population warranting the need for low doses, slow titration and frequent monitoring.13 A six-week trial period is advised by Fleminger et al (2006) to ascertain effects of treatment before trialling a new medication.4 Patient and family education regarding realistic treatment outcomes and side effects of treatments is also necessary to ensure treatment compliance.2 In future, a clarification of the underlying neurochemical changes is needed to identify further treatment targets. Additional larger scale RCTs are also needed to guide decision making and predict treatment outcomes. Table 2 offers a practical guide on medication choice in relation to aggressive behaviour in ABI.

References

  1. Tateno A, Jorge RE, Robinson RG. Clinical correlates of aggressive behaviour after traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2003;15(2):155-60.
  2. Kim E. Agitation, aggression and disinhibition syndromes after traumatic brain injury. NeuroRehabilitation 2002;17:297-310.
  3. Lombard LA, Zafonte RD. Agitation after traumatic brain injury: considerations and treatment options. Am J Phys Med Rehabil. 2005;84(10):797-812.
  4. Fleminger S, Greenwood RJ, Oliver DL. Pharmacological management for agitation and aggression in people with acquired brain injury. Cochrane Database Syst Rev. 2006;18(4):CD003299.
  5. Alderman N, Knight C, Brooks J. Rehabilitation Approaches to the Management of Aggressive Behaviour Disorders after Acquired Brain Injury. Brain Impairment. 2013;14(1):5-20.
  6. Siever LJ. Neurobiology of Aggression and Violence. Am J Psychiatry. 2008;165(4):429-42.
  7. McAllister TW. Neurobehavioral sequelae of traumatic brain injury: evaluation and management. World Psychiatry. 2008;7(1):3-10.
  8. Schwarzbold M, Diaz A, Martins ET, Rufino A, Amante LN, Thais ME et al. Psychiatric disorders and traumatic brain injury. Neuropsychiatr Dis Treat. 2008;4(4):797-816.
  9. Coccaro EF, Siever LJ. Pathophysiology and treatment of aggression. In: Davis KL, Charney D, Coyle JT, Nemeroff C, editors. Neuropsychopharmacology: The Fifth Generation of Progress. 5th ed. Pennsylvania: Lipincott, Williams & Wilkins; 2002:1709-23.
  10. Scottish Intercollegiate Guidelines Network. Brain injury rehabilitation in adults. Edinburgh: SIGN; 2013. 68 p. Report no.:130.
  11. Luauté J, Plantier D, Wiart L, Tell L, the SOFMER group. Care management of the agitation or aggressiveness crisis in patients with TBI. Systematic review of the literature and practice recommendations. Ann Phys Rehabil Med 2016;59(1):58-67.
  12. Warden DL, Gordon B, McAllister TW, Silver JM, Barth JT, Bruns J, et al. Guidelines for the Pharmacological Treatment of Neurobehavioral Sequelae of Traumatic Brain Injury. J Neurotrauma 2006;23(10):1468-501.
  13. Levy M, Berson A, Cook T, Bollegala N, Seto E, Tursanski S, et al. Treatment of agitation following traumatic brain injury: A review of the literature. NeuroRehabilitation 2005;20(4):279-306.
  14. Chew E, Zafonte RD. Pharmacological management of neurobehavioral disorders following traumatic brain injury – a state-of-the-art review. J Rehabil Res Dev 2009;46(6):851-79.

Anum Bhatti is currently in her final year of training for her MBchB at Keele University. She is interested in pursuing psychiatry as a career choice.

 

Dr George El-Nimr, MBChB, MSc (Neuropsych), MRCPsych, MSc (Psych), MMedEd, is a Consultant Neuropsychiatrist and Academic Secretary of the Faculty of Neuropsychiatry at the Royal College of Psychiatrists.

 

Correspondence to: Dr El-Nimr, Consultant Neuropsychiatrist, Neuropsychiatry Services, Bennett Centre, Richmond Terrace, Shelton, Stoke-on-Trent ST1 4ND. Tel: 01782 441614
Conflict of interest statement: None declared
Provenance and peer review: Submitted and externally reviewed
Date first submitted: 18/4/18
Date submitted after peer review: 21/9/18
Acceptance date: 15/5/19
To cite: Bhatti A, El-Nimr G. 
ACNR 2019;18(4);15-17
Published online: 1/8/19

via Pharmacological management of long-term aggression secondary to traumatic brain injuries | ACNR | Online Neurology Journal

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[WEB SITE] Can Ritalin Help Mitigate Brain Injury Symptoms?

Can Ritalin Help Mitigate Brain Injury Symptoms?

Question: 

My 54-year-old husband sustained a TBI when he fell asleep at the wheel while driving and hit a tree. The doctors say that he damaged all four parts of his brain. It’s been more than one and a half years and he’s still totally dependent on me to take care of him. Do you think Ritalin would help stimulate his brain?

Answer: 

Methylphenidate (Ritalin) is one of the commonly used brain stimulants in people who have suffered traumatic brain injury. It increases chemicals in the brain that have a stimulating effect (norepinephrine and dopamine).

After traumatic brain injury, doctors commonly prescribe Ritalin for low arousal or initiation, poor attention and concentration, depression, and slow processing speed. There is research that shows that Ritalin may speed recovery early after moderate to severe TBI. There is also research showing that Ritalin increases mental processing speed after TBI, which can improve memory function in some people.

All medications have side effects and the risks need to be weighed against possible benefits. One of the good things about the standard formulation of Ritalin is that it is short acting so if side effects occur they wear off in a few hours. Some potential side effects include keeping you up at night (if taken too close to bedtime), decreased appetite, headache, irritability, and paranoia.

In your husband’s case, his doctor needs to look at why he is so dependent. If arousal, attention, and/or initiation are playing a significant role, a stimulant can be considered. Careful monitoring for effects and/or side effects is needed when starting this medication and it should only be done by a doctor who has experience in caring for people with traumatic brain injury. Ritalin and most stimulants are controlled substances and will require frequent visits to the doctor for prescriptions.

Source: Can Ritalin Help Mitigate Brain Injury Symptoms? | BrainLine

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[WEB SITE] Efficacy of methylphenidate for the treatment of mental sequelae after traumatic brain injury

BACKGROUND: This study aimed to evaluate the effect of methylphenidate for treating mental sequelae after traumatic brain injury (TBI).
METHODS: Thirty-six patients with TBI were randomly divided into the intervention group and placebo group. The participants in the intervention group received methylphenidate, while subjects in the placebo group were administered a placebo.
This study was conducted from January 2014 to December 2016. The outcome measurements included Mental Fatigue Scale, Choice Reaction Time, Compensatory Tracking Task, Mental Arithmetic Test, Digit Symbol Substitution Test, Mini-Mental State Examination (MMSE), Beck Depression Inventory (BDI), and Hamilton Rating Scale for Depression. In addition, safety was also recorded and assessed.
RESULTS: A total of 33 subjects completed the study. Methylphenidate showed greater efficacy than placebo, with decreased scores on the Mental Fatigue Scale, Choice Reaction Time, and Compensatory Tracking Task in the intervention group compared to the placebo group (P < .01, respectively). Furthermore, increased scores on the Mental Arithmetic Test, Digit Symbol Substitution Test, and MMSE in the intervention group, compared to those in the placebo group (P < .01 respectively), were observed. In addition, a significant difference in the scores on the BDI (P = .04) and Hamilton Rating Scale for Depression (P = .005) was observed between the 2 groups. The safety at the end of the 30 week-treatment was similar between the 2 groups (P > .05).
CONCLUSION: The results of this study demonstrated that methylphenidate could effectively improve mental fatigue and cognitive functions in patients with TBI.

Source: Traumatic Brain Injury Resource Guide – Research Reports – Efficacy of methylphenidate for the treatment of mental sequelae after traumatic brain injury

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[WEB SITE] Can Ritalin Help Mitigate Brain Injury Symptoms?

 Question

My 54-year-old husband sustained a TBI when he fell asleep at the wheel while driving and hit a tree. The doctors say that he damaged all four parts of his brain. It’s been more than one and a half years and he’s still totally dependent on me to take care of him. Do you think Ritalin would help stimulate his brain?

Answer

Methylphenidate (Ritalin) is one of the commonly used brain stimulants in people who have suffered traumatic brain injury. It increases chemicals in the brain that have a stimulating effect (norepinephrine and dopamine).

After traumatic brain injury, doctors commonly prescribe Ritalin for low arousal or initiation, poor attention and concentration, depression, and slow processing speed. There is research that shows that Ritalin may speed recovery early after moderate to severe TBI. There is also research showing that Ritalin increases mental processing speed after TBI, which can improve memory function in some people.

All medications have side effects and the risks need to be weighed against possible benefits. One of the good things about the standard formulation of Ritalin is that it is short acting so if side effects occur they wear off in a few hours. Some potential side effects include keeping you up at night (if taken too close to bedtime), decreased appetite, headache, irritability, and paranoia.

In your husband’s case, his doctor needs to look at why he is so dependent. If arousalattention, and/or initiation are playing a significant role, a stimulant can be considered. Careful monitoring for effects and/or side effects is needed when starting this medication and it should only be done by a doctor who has experience in caring for people with traumatic brain injury. Ritalin and most stimulants are controlled substances and will require frequent visits to the doctor for prescriptions.

Source: Can Ritalin Help Mitigate Brain Injury Symptoms?

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[WEB SITE] New combinatination therapy shows promise in treating patients with traumatic brain injury

A combination of the stimulant drug methylphenidate with a process known as cognitive-behavioral rehabilitation is a promising option to help people who suffer from persistent cognitive problems following traumatic brain injury, researchers at Indiana University School of Medicine have reported.

The study, believed to be the first to systematically compare the combination therapy to alternative treatments, was published online in the journal Neuropsychopharmacology, a Nature publication.

The researchers, led by Brenna McDonald, PsyD, associate professor of radiology and imaging sciences, and Thomas McAllister, MD, chairman of the Department of Psychiatry, compared the effectiveness of two forms of cognitive therapy with and without the use of methylphenidate, a drug used to treat attention-deficit/hyperactivity disorder and better known by its trade name, Ritalin.

“We found that the combination of methylphenidate and Memory and Attention Adaptation Training resulted in significantly better results in attention, episodic and working memory, and executive functioning after traumatic brain injury,” said Dr. McDonald.

In the Memory and Attention Adaptation Training intervention – also used to assist patients with cognitive issues following breast cancer chemotherapy – therapists work with patients to help them develop behaviors and strategies to improve performance in memory and other cognitive tasks. In this study, this “metacognitive” approach was compared with Attention Builders Training, which Dr. McDonald likened to more of a “drill and practice” approach.

The 71 participants who completed the six-week trial were adults who had experienced a traumatic brain injury of at least mild severity – a blow to the head with some alteration of consciousness – at least four months previously, and who either complained of having cognitive problems, or who had been identified with cognitive problems in testing.

The participants were divided into four groups: the two cognitive therapy approaches with the drug therapy, and the two approaches with placebo. After six weeks, the researchers found that participants in the combination metacognitive-Ritalin group improved significantly better in word list learning, nonverbal learning and measures of attention-related and executive function.

However, Dr. McDonald cautioned that due to the relatively small number of participants in the each of the four arms of the trial – 17 to 19 people each – the results of the trial should be considered preliminary.

Nonetheless, she said, the work breaks new ground in providing evidence for the combination therapy.

“There have been a few small studies suggesting methylphenidate could help with attention and executive function after traumatic brain injury, which makes senses because it’s used to improve attention and focus. But this is the first to test it in combination with cognitive-behavioral therapy for treatment in traumatic brain injury,” said Dr. McDonald.

Source: Indiana University

Source: New combinatination therapy shows promise in treating patients with traumatic brain injury

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[WEB PAGE] Adding ADHD drug to therapy improves cognitive outcomes in traumatic brain injury patients

IMAGE

CREDIT: INDIANA UNIVERSITY SCHOOL OF MEDICINE

INDIANAPOLIS – A combination of the stimulant drug methylphenidate with a process known as cognitive-behavioral rehabilitation is a promising option to help people who suffer from persistent cognitive problems following traumatic brain injury, researchers at Indiana University School of Medicine have reported.

The study, believed to be the first to systematically compare the combination therapy to alternative treatments, was published online in the journal Neuropsychopharmacology, a Nature publication.

The researchers, led by Brenna McDonald, PsyD, associate professor of radiology and imaging sciences, and Thomas McAllister, MD, chairman of the Department of Psychiatry, compared the effectiveness of two forms of cognitive therapy with and without the use of methylphenidate, a drug used to treat attention-deficit/hyperactivity disorder and better known by its trade name, Ritalin.

“We found that the combination of methylphenidate and Memory and Attention Adaptation Training resulted in significantly better results in attention, episodic and working memory, and executive functioning after traumatic brain injury,” said Dr. McDonald.

In the Memory and Attention Adaptation Training intervention – also used to assist patients with cognitive issues following breast cancer chemotherapy – therapists work with patients to help them develop behaviors and strategies to improve performance in memory and other cognitive tasks. In this study, this “metacognitive” approach was compared with Attention Builders Training, which Dr. McDonald likened to more of a “drill and practice” approach.

The 71 participants who completed the six-week trial were adults who had experienced a traumatic brain injury of at least mild severity – a blow to the head with some alteration of consciousness – at least four months previously, and who either complained of having cognitive problems, or who had been identified with cognitive problems in testing.

The participants were divided into four groups: the two cognitive therapy approaches with the drug therapy, and the two approaches with placebo. After six weeks, the researchers found that participants in the combination metacognitive-Ritalin group improved significantly better in word list learning, nonverbal learning and measures of attention-related and executive function.

However, Dr. McDonald cautioned that due to the relatively small number of participants in the each of the four arms of the trial – 17 to 19 people each – the results of the trial should be considered preliminary.

Nonetheless, she said, the work breaks new ground in providing evidence for the combination therapy.

“There have been a few small studies suggesting methylphenidate could help with attention and executive function after traumatic brain injury, which makes senses because it’s used to improve attention and focus. But this is the first to test it in combination with cognitive-behavioral therapy for treatment in traumatic brain injury,” said Dr. McDonald.

###

In addition to Drs. McDonald and McAllister, researchers contributing to the study were Gwen C. Sprehn, Flora M. Hammond, Jaroslaw Harezlak, Li Xing, Rachel N. Wall, and Andrew J. Saykin of the IU School of Medicine; Laura A. Flashman, Carrie L. Kruck, and Karen L. Gillock of the Geisel School of Medicine, Dartmouth College; David B. Arciniegas of the Baylor College of Medicine; Robert J. Ferguson of the Department of Medicine, University of Pittsburgh; Arthur C. Maerlender of the University of Nebraska and Kim Frey of Craig Hospital, Englewood, Colorado.

This study was funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health (R01 HD047242). Dr. Arciniegas receives research support from the National Institute on Disability, Independent Living, and Rehabilitation Research (H133A120020, H133A130047) and Department of Veterans Affairs (CX000239) and receives compensation from American Psychiatric Association Publishing.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

Source: Adding ADHD drug to therapy improves cognitive outcomes in traumatic brain injury patients | EurekAlert! Science News

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[Abstract] Long-term treatment with methylphenidate for fatigue after traumatic brain injury – CNS

Acta Neurol Scand. 2016 Mar 15. doi: 10.1111/ane.12587.
OBJECTIVES: Traumatic brain injury (TBI) may cause long-lasting post-concussive symptoms, such as mental fatigue and concentration difficulties, and this may become the main hindrance for returning to work and studies. There is currently no effective treatment for long-lasting mental fatigue. In this hypothesis generating study, the long-term effects of methylphenidate on mental fatigue, cognitive function, and safety were assessed.
MATERIALS & METHODS: Thirty participants who suffered from long-term post-concussion symptoms after a mild TBI or moderate TBI and who had reported positive effects with methylphenidate during an initial phase of this follow-up study were treated with methylphenidate for a further six months.
RESULTS: After six-month follow-up, effects on Mental Fatigue Scale (MFS), depression, anxiety, and cognitive function (processing speed, attention, working memory) were significantly improved compared to baseline data (P < 0.001, respectively). Heart rate was significantly increased (P = 0.01), while blood pressure was not changed.
CONCLUSIONS: Individuals suffering from prolonged symptoms after TBI reported reduced mental fatigue and improved cognitive functions with long-term methylphenidate treatment. It is suggested that methylphenidate can be a treatment option for long-term mental fatigue and cognitive impairment after a TBI, but further randomized control research is warranted.

Source: Traumatic Brain Injury Resource Guide – Research Reports – Long-term treatment with methylphenidate for fatigue after traumatic brain injury

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